Hyperkalaemia in children
Hyperkalaemia is a potentially life-threatening electrolyte disturbance defined as a serum potassium level greater than 5.5 mmol/L in children and 6.0 mmol/L in neonates. Its primary danger lies in its effect on the cardiac conduction system, which can lead to fatal arrhythmias.
Aetiology
The causes of hyperkalaemia can be classified into four main categories.
Cellular Breakdown:
This is the most common cause of a spurious result. Haemolysis of a blood sample (e.g., from a prolonged tourniquet or difficult cannulation) releases potassium from red blood cells, giving a false high reading. Always confirm the result with a second, high-quality sample.
Tumour lysis syndrome: The rapid breakdown of cancer cells during chemotherapy.
Rhabdomyolysis: Muscle breakdown from crush injuries, severe burns, or prolonged seizures.
Decreased Renal Excretion: The kidneys are the primary route for potassium excretion.
Acute or chronic renal failure.
Drugs: ACE inhibitors, angiotensin receptor blockers (ARBs), and potassium-sparing diuretics (e.g., spironolactone).
Endocrine disorders: Adrenal insufficiency (Addison’s disease), which leads to a lack of aldosterone.
Increased Potassium Intake:
Iatrogenic causes, such as the inappropriate administration of potassium-containing IV fluids or oral supplements.
Extracellular Shift:
Acidosis: In metabolic acidosis, hydrogen ions move into cells, causing potassium to shift out.
Diabetic Ketoacidosis (DKA): The lack of insulin and an acidotic state causes a shift of potassium out of the cells. While total body potassium is low, the serum level can be high.
Clinical Presentation and Investigation
Clinical signs of hyperkalaemia can be subtle and non-specific, often not appearing until the condition is severe. Early signs may include paraesthesia, muscle weakness, and nausea. Cardiac arrhythmias can occur suddenly and without warning.
ECG: An electrocardiogram (ECG) is the most critical investigation and should be performed immediately. ECG changes are a direct reflection of cardiac toxicity and provide a guide for treatment.
Early changes: Tall, peaked T waves and a shortened QT interval.
Progressive changes: Flattened P waves, prolonged PR interval, and widening of the QRS complex.
Severe: A sine wave pattern, which can progress to ventricular fibrillation or asystole.
Other Investigations: Confirm the hyperkalaemia with a second blood sample. Check a blood gas to assess acid-base status, and measure renal function, glucose, and creatine kinase (CK).
Management Based on Severity
The UK approach to hyperkalaemia is a staged, time-critical response.
1. Mild Hyperkalaemia (K 5.5 – 6.0 mmol/L)
Action: Confirm the result with a second blood sample to rule out a false reading from haemolysis.
Treatment: Stop any potassium-containing fluids or medications (e.g., ACE inhibitors, potassium-sparing diuretics) and monitor the patient. Specific medical treatment is usually not needed unless the potassium continues to rise.
2. Moderate Hyperkalaemia (K 6.0 – 6.5 mmol/L) or Any ECG Changes
This is a medical emergency.
Action: Call for senior help and transfer the child to a monitored area (e.g., HDU or PICU). Immediately obtain a 12-lead ECG.
Treatment: The goal is to shift potassium into the cells and remove it from the body.
Intravenous Insulin and Glucose: This is the most effective way to cause an intracellular shift. A bolus of a fast-acting insulin (e.g., Actrapid) is given with a glucose infusion to prevent hypoglycaemia.
Nebulised Salbutamol: A high-dose nebulised beta-2 agonist can also rapidly shift potassium into cells.
Sodium Bicarbonate: Consider giving intravenous sodium bicarbonate if the child has a concurrent metabolic acidosis.
3. Severe Hyperkalaemia (K > 6.5 mmol/L) or Life-Threatening ECG Changes
This is a life-threatening emergency.
Action: Transfer to a monitored area and alert the PICU and anaesthetics teams.
Treatment: The immediate priority is cardiac protection.
Calcium Gluconate: Administer intravenous calcium gluconate or calcium chloride. Calcium rapidly stabilises the cardiac cell membranes and prevents arrhythmias. It does not lower the potassium level, so other treatments must be given concurrently.
Shift and Remove: Follow with the treatments for moderate hyperkalaemia (insulin-glucose, salbutamol).
Definitive Management: For refractory cases, consult with a paediatric nephrologist. Definitive removal of potassium requires haemodialysis or peritoneal dialysis.
Key Principles and Pitfalls
ECG is Key: The ECG is the single most important investigation as it indicates the level of cardiac toxicity. A normal ECG does not exclude risk, but a peaked T-wave or widened QRS complex is a clear sign for urgent treatment.
Rapid Treatment vs. Over-Correction: While swift action is needed, the overall correction should be slow to prevent a rapid fall in potassium, which can lead to arrhythmias.
Treat the Cause: Management is futile without identifying and addressing the underlying cause.